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Extensive editing of a small fraction of human T-cell leukemia virus type 1 genomes by four APOBEC3 cytidine deaminases

Renaud Mahieux^1,

Rodolphe Suspène^2,

Frédéric Delebecque^3,

¹ Unité d'Epidémiologie et Physiopathologie des Virus Oncogènes, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris cedex 15, France
² Unité de Rétrovirologie Moléculaire, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris cedex 15, France
³ G5 Virus et Immunité, Institut Pasteur, 28 rue du Dr Roux, 75724 Paris cedex 15, France

Correspondence
Jean-Pierre Vartanian
jpvart{at}pasteur.fr

In the absence of the human immunodeficiency virus type 1 (HIV-1) Vif protein, the host-cell cytidine deaminases APOBEC3F and -3G are co-packaged along with virion RNA. Upon infection of target cells, nascent single-stranded DNA can be edited extensively, invariably giving rise to defective genomes called GA hypermutants. Although human T-cell leukemia virus type 1 (HTLV-1) replicates in the same cell type as HIV-1, it was shown here that HTLV-1 is relatively resistant to the antiviral effects mediated by human APOBEC3B, -3C, -3F and -3G. Nonetheless, a small percentage of genomes (0·1<f<5 %) were edited extensively: up to 97 % of cytidine targets were deaminated. In contrast, hypermutated HTLV-1 genomes were not identified in peripheral blood mononuclear cell DNA from ten patients with non-malignant HTLV-1 infection. Thus, although HTLV-1 DNA can indeed be edited by at least four APOBEC3 cytidine deaminases in vitro, they are conspicuously absent in vivo.

Supplementary figures are available in JGV Online.

These authors contributed equally to this work.

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